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Natriuretic peptide measurement in non-heart failure settings

Horng H Chen, MD
Wilson S Colucci, MD
Section Editors
Stephen S Gottlieb, MD
Allan S Jaffe, MD
Deputy Editor
Susan B Yeon, MD, JD, FACC


The natriuretic peptide system impacts salt and water handling and pressure regulation and may influence myocardial structure and function.

Brain natriuretic peptide (BNP) is a natriuretic hormone initially identified in the brain but released primarily from the heart, particularly the ventricles. Cleavage of the prohormone proBNP produces biologically active 32 amino acid BNP as well as biologically inert 76 amino acid N-terminal pro-BNP (NT-proBNP).

Atrial natriuretic peptide (ANP) is a hormone that is released from myocardial cells in the atria and in some cases the ventricles in response to volume expansion and possibly increased wall stress [1]. ANP circulates primarily as a 28 amino acid polypeptide, consisting of amino acids 99 to 126 from the C-terminal end of its prohormone, pro-ANP.

The release of both ANP and BNP is increased in heart failure (HF), as ventricular cells are recruited to secrete both ANP and BNP in response to the high ventricular filling pressures [2]. The plasma concentrations of both hormones are increased in patients with asymptomatic and symptomatic left ventricular dysfunction, permitting their use in diagnosis (figure 1).

Natriuretic peptide levels are elevated in some patients with coronary heart disease, valvular heart disease, constrictive pericarditis, pulmonary hypertension, and sepsis (table 1). The diagnostic and prognostic value of measuring plasma BNP and NT-proBNP in asymptomatic individuals and patients with such non-HF conditions is discussed here. While the discussion here will focus on patients without overt HF, BNP or NT-proBNP elevations in some of these settings may be a sign of undiagnosed HF.

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Literature review current through: Nov 2017. | This topic last updated: Jun 23, 2016.
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